Cardio-oncology最新文献

{"title":"Ischemic heart disease and cardio-onco-hematology: a comprehensive review.","authors":"Santiago Jiménez-Marrero, Herminio Morillas, Alexandra Pons-Riverola, Alberto Garay, Raul Ramos-Polo, Javier Berdejo, Encarnación Hidalgo, Cristina Enjuanes, Josep Comín-Colet, Pedro Moliner Borja","doi":"10.1186/s40959-026-00521-y","DOIUrl":"10.1186/s40959-026-00521-y","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular disease and cancer represent the leading causes of mortality worldwide. The coexistence of ischemic heart disease and cancer is increasing due to shared risk factors, improved cancer survival, and cardiovascular toxicity from antineoplastic treatments. This complex relationship poses unique diagnostic and therapeutic challenges requiring multidisciplinary management approaches.</p><p><strong>Main body: </strong>This comprehensive review examines the multifaceted relationship between ischemic heart disease and cancer, analyzing firstly shared risk factors including smoking, sedentary lifestyle, obesity, diabetes, dyslipidemia and hypertension. We discuss the pathophysiological mechanisms linking cancer and ischemic heart disease, particularly chronic inflammatory states and prothrombotic conditions. The review systematically evaluates cardiovascular toxicity associated with major cancer therapies, including chemotherapy (fluoropyrimidines, platinum compounds, proteasome inhibitors), targeted therapy (vascular endothelial growth factor inhibitors), radiotherapy, immunotherapy, and hormonal treatments. We address the clinical presentation spectrum from asymptomatic ischemia to acute coronary syndromes, highlighting diagnostic challenges and management particularities in cancer patients. Special attention is given to the management of patients with thrombocytopenia and the specific case of fluoropyrimidine-induced cardiotoxicity.</p><p><strong>Conclusions: </strong>The intersection of ischemic heart disease and cancer requires specialized cardio-oncology expertise to optimize both cancer treatment and cardiovascular outcomes. Early cardiovascular risk stratification, careful selection of cancer therapies, and coordinated multidisciplinary care are essential. As cancer survivorship continues to improve, long-term cardiovascular monitoring and risk factor modification become increasingly important. Future research should focus on developing predictive biomarkers, cardioprotective strategies, and evidence-based guidelines to better manage this complex patient population.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal trends and forecasted mortality involving lung cancer with co-listed hypertension in U.S. adults, 2000-2035.","authors":"Syeda Samia Fatima, Asma Naz, Muneeb Fareed, Muhammad Hussain, Fnu Arsheen, Nisha Khalid, Muhammad Hassan, Fnu Pirih, S M Aleem Hussain, Saifullah Khan, Hasibullah Aminpoor","doi":"10.1186/s40959-026-00524-9","DOIUrl":"10.1186/s40959-026-00524-9","url":null,"abstract":"<p><strong>Background: </strong>Lung Cancer (LC) and Hypertension (HTN) frequently co-exist as a significant comorbidity with shared risk factors and pathophysiological mechanisms. We examined national trends and forecast future mortality involving LC co-listed with HTN among US adults from 2000 to 2025, with projections to 2035.</p><p><strong>Methods: </strong>Using CDC WONDER MULTIPLE Cause-of-Death, we conducted a retrospective analysis of LC and co-listed HTN mortality from 2000 to 2025 among adults aged ≥ 25 years. Age-adjusted mortality rates (AAMRs) were calculated, and joinpoint regression was utilized to estimate annual average percentage changes (AAPCs) with 95% confidence intervals (CIs). Auto-ARIMA and Prophet time-series models in R (v4.5.0) projected AAMRs through 2035, evaluated by root mean squared error (RMSE).</p><p><strong>Results: </strong>There were 305,878 reported deaths due to LC and co-listed HTN. The AAMR rose from 3.55 to 6.00 (AAPC 2.038; p < 0.0001). Men had higher mean AAMRs than women (mean AAMR: men 6.16; women 4.07). Among races, Non-Hispanic (NH) Black adults had the greatest mortality (mean AAMR: 7.38). Geographically, the South had the greatest burden (mean AAMR: 5.67) and non-metropolitan regions had higher mean AAMR than metropolitan regions (5.73 vs. 4.5). Most deaths (42.16%) occurred in decedents' homes. The overall AAMR was projected to remain persistently elevated through 2035, particularly among men, NH White individuals, and in the Southern region with substantial uncertainty.</p><p><strong>Conclusion: </strong>Mortality associated with LC and co-listed HTN is an increasing healthcare burden in the US with marked demographic and regional disparities. Future projections indicate a persistent mortality burden, underscoring the need for targeted prevention strategies.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148283469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A rare case of fulminant talquetamab-induced myocarditis presenting as a STEMI mimicker.","authors":"Eric J Kim, Sara Diaz Saravia, Gagan Sahni","doi":"10.1186/s40959-026-00535-6","DOIUrl":"10.1186/s40959-026-00535-6","url":null,"abstract":"<p><strong>Background: </strong>Immune-mediated myocarditis is a rare and potentially fatal complication of oncologic immunotherapy. While most reported cases have been associated with the use of immune checkpoint inhibitors (ICIs), novel immunotherapy agents may also pose cardiac risks that warrant further attention. We report a case of fulminant, steroid-refractory myocarditis following initiation of talquetamab, a bispecific T-cell engager (BiTE) targeting CD3 and GPRC5D used for relapsed or refractory multiple myeloma (MM).</p><p><strong>Case presentation: </strong>A 69-year-old man with MM refractory to multiple lines of treatment presented to his outpatient cardio-oncologist with syncope and intermittent chest pain 4 weeks after starting talquetamab. He was found to have elevated high-sensitivity troponin and new inferior Q waves on EKG. He presented to the hospital, where he was admitted to the cardiac intensive care unit. New ST-segment elevations in the inferior leads were subsequently observed on serial EKGs. Transthoracic echocardiography showed a decreased left ventricular (LV) ejection fraction with new regional wall motion abnormalities. Left and right heart catheterization and endomyocardial biopsy were unremarkable. Cardiac magnetic resonance imaging (MRI) revealed segmental late gadolinium enhancement, myocardial edema, increased T1 time, and increased extracellular volume. Acute myocarditis due to talquetamab was presumed, and intravenous steroid therapy was initiated. His symptoms and biomarkers initially improved but later worsened despite steroid therapy. He received additional immunosuppressive therapies including tocilizumab, mycophenolate mofetil, intravenous immunoglobulin, and ruxolitinib. However, his biomarkers and LV systolic function continued to worsen, ultimately resulting in death.</p><p><strong>Conclusions: </strong>This case underscores the potential for immune-mediated myocarditis associated with talquetamab to follow a fulminant and treatment-refractory course despite guideline-directed escalation of immunosuppression, with important implications for clinical recognition and management. It also illustrates the diagnostic challenge of immune-mediated myocarditis presenting as an ST-segment elevation myocardial infarction (STEMI) mimic with non-obstructive coronary arteries. Finally, it emphasizes the complementary role of cardiac MRI in establishing the diagnosis when endomyocardial biopsy is non-diagnostic.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148283482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A systematic review of artificial intelligence in radiotherapy associated cardiovascular toxicity.","authors":"Vivian Salama, Brandon M Godinich, Nathaniel Dunham, Troy Nguyen, Sijin Wen, Joseph A Schmidlen, Wesley Cox, Peyton M Lilly, Jeffrey Ryckman, Ramon Alfredo Siochi, Ashkan Emadi, Christopher M Bianco, George G Sokos, Raymond R Raylman, David A Clump, Mina F Hanna, Phillip M Pifer","doi":"10.1186/s40959-026-00528-5","DOIUrl":"10.1186/s40959-026-00528-5","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular toxicity (CVT) is a major concern after radiotherapy (RT), contributing to morbidity and mortality among cancer survivors. Artificial intelligence (AI) may improve risk prediction and RT planning; however, its role in RT-associated CVT remains unclear. This study aimed to systematically evaluate AI applications and study quality in this field.</p><p><strong>Methods: </strong>A PRISMA-guided systematic review of PubMed, Ovid EMBASE, Cochrane Library, and Web of Science was conducted through October 1, 2025. Eligible studies included original human research in English applying AI to CVT or imaging in cancer populations receiving RT. Predictive and imaging studies were evaluated using TRIPOD + AI/PROBAST and CLAIM/QUADAS-2, respectively. Exploratory meta-analysis of performance metrics was conducted where feasible.</p><p><strong>Results: </strong>Sixty-five studies were included, comprising AI prediction models (n = 31, 48%) and cardiovascular imaging applications (n = 34, 52%). Deep learning was the most common approach (45/65, 69%) and demonstrated the highest predictive performance (median AUC = 0.82; median sensitivity = 0.83). Calibration assessment (3/31, 10%) and external validation (6/31, 19%) were limited. Meta-analysis demonstrated an overall predictive model accuracy of 0.83 (95% CI: 0.77-0.87). Imaging models performed well for larger cardiac structures (overall median DSC = 0.85, range: 0.76-0.94), while coronary artery segmentation remained challenging. Average TRIPOD + AI and CLAIM adherence were 79% and 71%, respectively. Most predictive (97%) and imaging (82%) studies were rated at high risk-of-bias.</p><p><strong>Conclusion: </strong>AI shows promise for RT-associated CVT prediction and imaging but is underdeveloped for routine clinical implementation. Heterogeneity, limited validation, and methodological limitations highlight the need for standardized endpoints, external validation, and prospective clinical evaluation.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental endocrine disruptors in cardio-oncology: emerging modifiers of cardiovascular vulnerability in patients with cancer.","authors":"Vincenzo Quagliariello, Massimiliano Berretta, Giuseppe D'Aiuto, Irma Bisceglia, Matteo Barbato, Benedetta Del Toro, Jacopo Santagata, Maria Laura Canale, Andrea Paccone, Alessandro Inno, Cristiana D'Ambrosio, Stefano Oliva, Christian Cadeddu Dessalvi, Tiziana Di Matola, Domenico Gabrielli, Iacopo Fabiani, Leopoldo Pagliani, Cezar A Iliescu, Anna Borowiec, Nicola Maurea","doi":"10.1186/s40959-026-00532-9","DOIUrl":"10.1186/s40959-026-00532-9","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Cardio-oncology has traditionally focused on treatment-related cardiovascular toxicity and conventional cardiovascular risk factors. However, increasing evidence suggests that environmental exposures may contribute to both cancer development and cardiovascular disease through shared biological mechanisms. Endocrine-disrupting chemicals (EDCs) are ubiquitous environmental contaminants capable of interfering with hormonal signaling, metabolic homeostasis, vascular function, and inflammatory pathways. Despite growing evidence linking EDCs to cardiometabolic disorders and hormone-sensitive malignancies, their potential role within the cardio-oncology continuum remains largely unexplored.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This narrative review summarizes and critically discusses current experimental, translational, and epidemiological evidence regarding the potential contribution of environmental endocrine disruptors to cardiovascular risk and cancer biology. Particular attention is given to molecular pathways relevant to cancer therapy-related cardiovascular toxicity, breast cancer biology, adipose tissue dysfunction, and emerging exposomic determinants of long-term cardiovascular outcomes in patients with cancer.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main body: &lt;/strong&gt;Major classes of EDCs, including bisphenols, phthalates, per- and polyfluoroalkyl substances (PFAS), persistent organic pollutants (POPs), parabens, pesticides, and other environmental contaminants, are continuously encountered through food systems, plastics, consumer products, contaminated water, and healthcare materials. These compounds influence multiple biological processes that are central to both oncogenesis and cardiovascular disease, including oxidative stress, mitochondrial dysfunction, endothelial injury, chronic inflammation, metabolic reprogramming, thrombosis, and epigenetic remodeling. In breast cancer, EDCs may modulate subtype-specific signaling pathways involving estrogen receptor activation, HER2 crosstalk, aryl hydrocarbon receptor signaling, and homologous recombination networks. In parallel, growing evidence supports associations between EDC exposure and hypertension, accelerated atherosclerosis, heart failure, metabolic syndrome, and major adverse cardiovascular events. We further discuss the hypothesis that lipophilic EDCs may accumulate within adipose depots and that dysfunctional epicardial adipose tissue could represent a local toxicological niche capable of amplifying cardiovascular vulnerability in cancer survivors, although direct evidence remains unavailable.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;EDCs should not yet be considered established cardio-oncology risk factors; however, they represent biologically plausible exposomic modifiers operating at the intersection of cancer, metabolism, and cardiovascular disease. Incorporating environmental exposures into cardio-oncology research may improve understanding of interindividual variability in cardiova","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13289265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac dysfunction during immune checkpoint inhibitor therapy: association with extracardiac immune-related adverse events.","authors":"Raluca I Mincu, Lena Lampe, Lars Michel, Amir A Mahabadi, Adelina V Mark, Lisa Zimmer, Elisabeth Livingstone, Dirk Schadendorf, Alpaslan Tasdogan, Tienush Rassaf, Matthias Totzeck","doi":"10.1186/s40959-026-00529-4","DOIUrl":"10.1186/s40959-026-00529-4","url":null,"abstract":"<p><strong>Background and aims: </strong>With the increasing approval of immune checkpoint inhibitors (ICI) for cancer treatment, there is a rising incidence of potentially life-threatening cancer-therapy related cardiac dysfunction (CTRCD). Current 2022 European Society of Cardiology (ESC) guidelines on cardio-oncology recommend a single baseline transthoracic echocardiogram (TTE) for high-risk ICI-treated patients, potentially underestimating the incidence of CTRCD due to lack of follow-up assessments. This study aims to characterize the incidence of CTRCD in cancer patients undergoing ICI therapy using an intensified TTE surveillance approach and to investigate whether extracardiac immune-related adverse events (eirAEs) are associated with CTRCD.</p><p><strong>Methods: </strong>We analysed patients scheduled for ICI therapy from the Essen Cardio-Oncology Registry (EcoR). Data were collected during cardio-oncology consultations at baseline, 6 weeks, 6 months, and 12 months. Patients with eirAEs were evaluated compared to patients without eirAEs.</p><p><strong>Results: </strong>Among 2,540 cancer patients registered in EcoR until march 2023, 266 (61 ± 14 years, 40.6% female, 86.5% melanoma, 62% metastatic disease) were scheduled for ICI therapy. CTRCD was observed in 35.7% of patients, with 32.7% having asymptomatic mild CTRCD, 0.37% moderate CTRCD, and 2.63% developing heart failure with preserved ejection fraction (HFpEF). Patients with eirAEs had a twofold higher risk of CTRCD (relative risk [RR] 2.05, 95% CI: 1.49-2.83, p < 0.001) and a 66% increased risk of cardiovascular toxicity (RR 1.66, 95% CI 1.30-2.13, p < 0.001).</p><p><strong>Conclusions: </strong>ICI therapy is associated with a high prevalence of CTRCD, underscoring the importance of serial echocardiography evaluation, particularly for patients with eirAEs. Enhanced cardio-oncology surveillance is crucial for improving patient outcomes and survival.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"12 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13270561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effective management of 5-fluorouracil-induced coronary vasospasm allowing chemotherapy continuation: a single-center observational study.","authors":"Kinga Kolossváry, Krisztina Heltai, Borbála Székely, Gábor Rubovszky","doi":"10.1186/s40959-026-00526-7","DOIUrl":"10.1186/s40959-026-00526-7","url":null,"abstract":"<p><strong>Background: </strong>5-fluorouracil (5-FU) is a widely used chemotherapy agent in gastrointestinal (GI) malignancies, but it can cause cardiotoxicity, most commonly manifesting as chest pain due to coronary vasospasm, often mimicking acute coronary syndrome. Adequate management of 5-FU-associated vasospasm is critical to ensure the necessary oncological treatment can be safely continued.</p><p><strong>Objectives: </strong>The aim of this study was the retrospective analysis of cases of chest pain associated with intravenous 5-FU treatment in GI cancer patients at a single institution, and to report the experiences with antianginal treatment, specifically nitrates and calcium channel blockers, administered in these cases.</p><p><strong>Methods: </strong>This was a retrospective, single-center, observational cohort study. We analyzed data of GI cancer patients treated with intravenous 5-FU between March 2024 and August 2025 who experienced chest pain during treatment. Following the institutional protocol, the chemotherapy was transiently suspended, and treatment was re-introduced under combined oral or intravenous nitrate and calcium channel blocker protection.</p><p><strong>Results: </strong>Out of 835 patients receiving iv 5-FU, 25 (2.9%) developed chest pain, typically after the second or third cycle of chemotherapy. Three patients presented with ST-elevation on ECG, but none of them showed significant coronary stenosis on imaging. With appropriate cardiological treatment, all 25 patients achieved symptom-free oncological treatment continuation: 19 patients with combined nitrate and calcium channel blocker therapy, 6 with monotherapy, and one of these patients required intravenous treatment under ICU monitoring.</p><p><strong>Conclusions: </strong>Coronary vasospasm associated with intravenous 5-FU is a rare but clinically significant complication. Our findings, in line with the literature, suggest that the introduction of antianginal therapy successfully allowed the safe rechallenge and continuation of oncological therapy in all affected patients, which may prevent unnecessary discontinuation of life-prolonging chemotherapy.</p><p><strong>Trial registration: </strong>Retrospectively registered (Approval No. OOI/Ált11147-1/2025).</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heterogeneity in proportional cardiovascular co-listing on cancer death certificates in the United States: a national multiple cause-of-death analysis, 1999-2020.","authors":"Faizan Ahmed, Tehmasp Rehman Mirza, Yusra Junaid, Hassaan Abid, Haris Bin Tahir, Areehah Zafar Masood, Zaima Afzaal, Gabriel Benjamen, Brijesh Patel","doi":"10.1186/s40959-026-00525-8","DOIUrl":"10.1186/s40959-026-00525-8","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular disease (CVD) and cancer share common risk factors, and cancer survivors experience elevated long-term cardiotoxicity. Traditional risk-based metrics require person-time denominators that are unavailable in aggregate public health databases. This study introduces a proportional co-listing framework to detect population-level cardiovascular surveillance signals on death certificates across cancer types and demographic strata.</p><p><strong>Methods: </strong>We conducted a national cross-sectional surveillance analysis using CDC WONDER Multiple Cause-of-Death data from 1999 to 2020 for decedents aged ≥ 15 years. Utilizing an \"any-mention\" framework, we calculated the Proportional Mortality Ratio (PMR), defined as the ratio of CVD co-listing on cancer-related death certificates to CVD listing on non-cancer certificates. Temporal trends were evaluated using joinpoint regression to estimate the average annual percent change (AAPC). Analyses were stratified by age, sex, race/ethnicity, geography, and index cancer subtypes (lung, colon, and leukaemia).</p><p><strong>Results: </strong>Of 56,014,102 death certificates analyzed, 13,917,133 (24.8%) listed a malignant neoplasm, of which 3,997,238 (28.7%) co-listed CVD. Across the lifespan, the overall PMR followed a reverse J-shaped curve. Proportional co-listing was highest in the youngest cohort (ages 15-24: PMR 1.828, 95% CI: 1.778-1.879), declined to a nadir at ages 55-64 (PMR 0.336, 95% CI: 0.335-0.337), and rose modestly in older adulthood. From 1999 to 2020, PMRs increased significantly across all adult age groups, peaking at ages 55-64 (AAPC 1.69%, 95% CI: 1.52-1.83, p < 0.001). Young-adult PMR elevations were consistently higher in male, metropolitan, and Hispanic/Latino decedents. Among subtypes, leukaemia demonstrated the highest relative CVD co-listing in young adults (PMR 2.174), whereas colon cancer showed no statistically significant elevation (PMR 1.173, 95% CI: 0.951-1.447).</p><p><strong>Conclusions: </strong>Cardiovascular co-listing on US cancer death certificates is highly patterned by age, demographics, and cancer subtype. While elevated PMRs in young adults are consistent with patterns previously reported in cardio-oncology literature, sub-unity PMRs in middle-aged and older adults may reflect under-documentation of cardiovascular comorbidities in oncology settings alongside denominator effects arising from frequent CVD listing on non-cancer certificates. Improving comorbidity documentation on death certificates may enhance the utility of national administrative data for cardio-oncology surveillance and research.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13651163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends and disparities for co-existent pancreatic cancer and cardiovascular-related deaths: a retrospective 1999-2020 analysis of CDC WONDER data.","authors":"Rohit B Ponnada, Atman K Shah, Atharva M Bhagwat, Bhanuteja Pujari, Chien-Jung Lin","doi":"10.1186/s40959-026-00497-9","DOIUrl":"10.1186/s40959-026-00497-9","url":null,"abstract":"<p><strong>Purpose: </strong>Pancreatic cancer and cardiovascular disease are among the leading causes of death in the U.S. and may co-occur with compounding effects. This study assesses trends in mortality rates for comorbid pancreatic cancer and cardiovascular disease, along with sociodemographic disparities to better inform public health and policy efforts.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted using CDC WONDER data between 1999 and 2020. Mortality for pancreatic cancer was assessed using ICD-10 code C25 with I00-I99 for any cardiovascular-related death. Joinpoint regression software was used to assess mortality trends overall and across strata of race, sex, and urbanization status. Age-adjusted mortality rate (AAMR) per 1,000,000 was examined on a year-by-year and demographic basis by assessing annual percent change (APC) with confidence intervals and p-values.</p><p><strong>Results: </strong>Between 1999 and 2020, 189,463 deaths were associated with both cardiovascular death and pancreatic cancer. Overall age-adjusted mortality rate (AAMR) per 1,000,000 increased from 26.164 in 1999 to 31.478 in 2020 (APC = 0.85%, CI = 0.72-0.98%, p < 10⁻⁶). Males consistently had higher mortality rates than females, with both groups showing significant increases (APC_male=0.86%, APC_female=0.94%, p < 10⁻⁶). White individuals had higher absolute mortality rates, whereas Black/African-American individuals demonstrated a greater relative increase over time (APC = 1.38% vs. 1.10%; p < 10⁻⁶ for both). Metropolitan residents had consistently lower mortality rates than non-metropolitan residents, but metropolitan residents experienced a sharper increase (APC_metro=0.84%, APC_non-metro=0.63%, p < 10⁻⁶).</p><p><strong>Conclusions: </strong>Pancreatic cancer-associated cardiovascular mortality has consistently increased in the United States from 1999 to 2020. There were notable demographic disparities which could provide insight towards targeted interventions for long-term mortality decrease.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13474661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148216638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic and prognostic biomarkers in heart failure and myeloproliferative neoplasms: clinical applications and risk scores - a narrative review.","authors":"Ionela-Raluca Muraretu, Adriana Luminita Gurghean, Adrian Gradinaru, Mircea Bajdechi, Ilinca Savulescu-Fiedler, Anca-Maria Mihailescu, Adriana Mihaela Iliesiu","doi":"10.1186/s40959-026-00518-7","DOIUrl":"10.1186/s40959-026-00518-7","url":null,"abstract":"<p><p>Heart failure (HF) remains a leading cause of morbidity and mortality worldwide and frequently coexists with Philadelphia-negative myeloproliferative neoplasms (MPNs), which share thrombo-inflammatory pathways that increase cardiovascular risk. HF is often underestimated in this population, and current risk models rarely include variables specific to this complex cardio-hematologic setting. From a cardio-oncology perspective, MPNs represent a prototypical at-risk cancer population in whom chronic inflammation, clonal hematopoiesis, and cancer therapy converge to accelerate cardiovascular damage.This narrative review summarizes current evidence on diagnostic and prognostic biomarkers, imaging parameters, and validated HF and MPNs risk scores, and proposes a pragmatic hybrid framework for integrated HF-MPNs cardiovascular risk assessment. PubMed, Embase, and Web of Science were searched up to December 2025 using combinations of terms related to HF, MPNs, biomarkers, imaging, and risk models. In HF, natriuretic peptides and cardiac troponins remain central for diagnosis and short-term prognosis, whereas emerging biomarkers such as galectin-3, soluble ST2, and GDF-15 refine long-term risk prediction. Advanced imaging tools, including global longitudinal strain, left atrial strain, and cardiac magnetic resonance tissue characterization, provide prognostic value beyond the left ventricular ejection fraction. Multidimensional HF models (e.g., MAGGIC, SHFM, BCN Bio-HF, H2FPEF, 3A3B, GWTG-HF, ADHERE, and EHMRG) combine different variables to estimate mortality and hospitalization risk. In MPNs, blood counts, driver mutations (JAK2, CALR, MPL), inflammatory markers, and scores such as IPSET-thrombosis, DIPSS/DIPSS-plus, and MIPSS stratify thrombotic risk, survival, and leukemic transformation but seldom incorporate HF-specific variables.No single biomarker or score fully captures the bidirectional cardiovascular risk in patients with HF and coexisting MPNs. We propose a simple 0-8-point composite algorithm that combines key HF and MPNs variables (natriuretic peptides or troponins, HF risk scores, driver mutations, leukocytosis/thrombocytosis, LDH) to identify high-risk HF-MPNs phenotypes across ACC/AHA HF Stages A-C, suitable for structured cardio-oncology follow-up. Prospective validation of this hybrid algorithm in dedicated cardio-oncology cohorts and the development of MPNs-adapted HF guidelines are key future priorities.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13422315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148194664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}